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Should I Eat Gluten Before Testing?

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I am on a gluten free diet right now. I will get tested for Celiac this weekend. I have heard that I should eat something that contains gluten before the test otherwise it may not detect the disease. So how long before the test should I start eating gluten? A day? A week? I need some professional feedback.

Thank you!

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It depends a lot on how long you have been gluten free. The usual recommendation is that you should have been eating something like the equivalent of three-four slices of bread for at least three months before the tests, but if you've only been gluten free for a couple weeks it's probably enough to just start eating gluten now. If it's been longer I'm afraid it might be too late to start now, and your test results may be unreliable. :(

It also might depend on the test you're having, are you having blood drawn or going for a biopsy? Some people always test negative on the blood tests, but they may still have a positive biopsy. Some people still have antibodies in their blood and some damage that can be found in the biopsy after two years gluten free, but other people might test negative very quickly after going gluten free. That depends on how your immune system works and how quickly you heal, so it's a very individual thing and it's impossible to give a hard and fast rule. That's why the basic idea is that it's best to eat gluten all the way until all the testing is completed, to make the chances of false negatives smaller.

Pauliina

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You should be eating a normal gluten filled diet for a few weeks-few months before testing. The purpose of the testing is to detect damage. Damage doesn't occur overnight, and the bloodwork accuracy has been correlated to the level of villi damage. Meaning, lower levels of damage (if you have Celiac) may not reflect in blood testing.

The goal of the diet is to heal the damage, and have the repeat bloodwork/biopsies look "normal" - which is what happens when most people who have Celiac go gluten free. Eating gluten free and having the testing done can result in false negatives.

What has your doctor said about this?

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It depends on which blood tests are being run, and how long you've been gluten free.

I have been trying to stay gluten free for a few months. But it's hard to avoid gluten eating at a university dining hall. So I might have eaten gluten without knowing. I avoid eating bread and other food that obviously have gluten. But there might be cross-contamination and other things. So I wouldn't say I am eating a completely free-of-gluten diet.

I am going to the Celiac Center of University of Chicago, they have an annual free screening. I think the blood test is Anti-Tissue Transglutaminase (tTG-IgA) , but I am not positive.

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I have heard that you should have been eating gluten for several days before your test.

I'm' not positive though.

Have you asked your doctor?

I am on a gluten free diet right now. I will get tested for Celiac this weekend. I have heard that I should eat something that contains gluten before the test otherwise it may not detect the disease. So how long before the test should I start eating gluten? A day? A week? I need some professional feedback.

Thank you!

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You should be eating a normal gluten filled diet for a few weeks-few months before testing. The purpose of the testing is to detect damage. Damage doesn't occur overnight, and the bloodwork accuracy has been correlated to the level of villi damage. Meaning, lower levels of damage (if you have Celiac) may not reflect in blood testing.

The goal of the diet is to heal the damage, and have the repeat bloodwork/biopsies look "normal" - which is what happens when most people who have Celiac go gluten free. Eating gluten free and having the testing done can result in false negatives.

What has your doctor said about this?

Do you have a link to one of the studies correlating bloodwork accuracy and villi damage? Not doubting you but that's one of the areas I'd like to know more about - especially as it relates to false results.

Thank you.

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Some of my references include:

http://www.ncbi.nlm.nih.gov/pubmed/1833335...pt=AbstractPlus

Rom J Intern Med. 2007;45(3):263-8.Links

Serological and histological correlations in celiac disease.Tărmure S, Cristea A, Sămpelean D, Negrean V, Alexescu T.

14th Medical Clinic, "Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania. starmure@hotmail.com

The aim of this study was to compare the sensitivity of the serological markers in patients with non-treated celiac disease by determination of antiendomysium and anti-tissue-transglutaminase autoantibodies separately and together. At the same time we examined the correlation between the serum levels of the two antibodies and the severity of the histological lesions. MATERIAL AND METHODS: The research included 26 persons (19 females, 7 males, age range 18-56 years) in whom the small bowel biopsy confirmed the villous atrophy. The sera of these patients were investigated by the determination of antiendomysium antibodies (AEA) and antitissue-transglutaminase antibodies (ATTG). For the morphological disorders we used the Marsh modified criteria. ATTG were determined by a sandwich-ELISA technique and AEA were dosed by indirect immunofluorescence technique. RESULTS: 6 patients presented with partial villous atrophy (PVA), 7 with subtotal villous atrophy (SVA) and 13 with total villous atrophy (TVA). 23 persons were seropositive, having at least one of the two antibodies tested. The sensitivity of the serological investigation increased at 88% using both AEA and ATTG determinations. In patients with TVA, the sensitivity of ATTG was 100% and of AEA was 92%. In patients with SVA and PVA, the sensitivity of these antibodies was lower. Among the patients with SVA, 43% were negative for AEA and 50% for ATTG. The determination of AEA and ATTG together reduced the seronegativity at 15% in patients with SVA and at 34% in patients with PVA. CONCLUSIONS: Antitissue-transglutaminase antibodies testing in patients with non-treated celiac disease is more sensitive than antiendomysium antibodies. The efficiency of the serological diagnosis improves when both AEA and ATTG are determined. Serum antibodies levels correlated very well with the severe histological alterations (TVA), but the correlation is not so good with SVA and PVA. So, we can tell that high levels of AEA and/or ATTG are suggestive for severe histological disorders in celiac disease.

http://www.ncbi.nlm.nih.gov/pubmed/11374690?dopt=Abstract

Am J Gastroenterol. 2001 May;96(5):1507-10.Related Articles, Links

Low prevalence of antigliadin and anti-endomysium antibodies in subclinical/silent celiac disease.

Tursi A, Brandimarte G, Giorgetti G, Gigliobianco A, Lombardi D, Gasbarrini G.

Division of Internal Medicine, Umberto I Hospital, Barletta, Italy.

OBJECTIVE: Endomysial antibodies (EMA) are a well-known hallmark of celiac disease, but some recent studies showed that the prevalence of these antibodies in clinical practice is lower than expected. The aim of our study was to determine the prevalence of antigliadin (AGA) and EMA antibodies on a consecutive series of subclinical/silent celiac patients. METHODS: We studied 115 consecutive patients with subclinical (92 patients) or silent (23 patients) forms of celiac disease. AGA and EMA were screened in all patients. Histopathology of celiac disease was expressed according to the Marsh classification. RESULTS: The overall AGA in subclinical form were positive in 77% (14 of 18) of patients with partial villous atrophy (VA), in 84% (21 of 25) of patients with subtotal VA, and in 90% (27 of 30) of patients with total VA, whereas EMA were positive in 88.88% (16 of 18) of patients with partial VA, in 92% (23 of 25) of patients with subtotal VA, and 96.66% (29 of 30) of patients with total VA. On the other hand, AGA were positive in 0% (zero of two) of patients with Marsh I and in 30% (three of 10) of patients with Marsh II, whereas EMA were positive in 0% (zero of two) of patients with Marsh I and in 40% (four of 10) of patients with Marsh II (Marsh I-IIIa vs Marsh IIIb-c, p = < 0.005 in overall AGA-positive patients and p = < 0.0001 in EMA-positive patients). At the same time the overall AGA in silent form were positive in 60% (three of five) of patients with partial VA, in 66.66% (four of six) of patients with subtotal VA, and in 77.77% (seven of nine) of patients with total VA, whereas EMA were positive in 80% (four of five) of patients with partial VA, in 83.33% (five of six) of patients with subtotal VA, and in 88.88% (eight of nine) of patients with total VA. On the other hand, overall AGA were positive in 0% of patients with both Marsh I (zero of one) and Marsh II (zero of two), as well as EMA were positive in 0% with both Marsh I (zero of one) and Marsh II (zero of two) (Marsh I-IIIa vs Marsh IIIb-c, p = < 0.001 in overall AGA-positive patients and p = < 0.007 in EMA-positive patients). CONCLUSIONS: At this time small bowel biopsy seems to be the only correct procedure to diagnose a case of suspected celiac disease, especially in patients with mild symptoms or suspected for celiac disease, because they belong to high-risk groups.

PMID: 11374690 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/11374690?dopt=Abstract

Rom J Gastroenterol. 2003 Jun;12(2):101-6.Related Articles, Links

Autoantibodies and histogenesis of celiac disease.

Rostami K, Mulder CJ, Stapel S, von Blomberg BM, Kerckhaert J, Meijer JW, Peńa SA, Heymans HS.

Department of Gastroenterology Withybush General Hospital, Pembrokeshire, Haverfordwest, UK. krostami@hotmail.com.

OBJECTIVE: Autoantibodies are used as markers for celiac disease (celiac disease) identifying patients with mucosal lesions. The purpose of this study was to evaluate the sensitivity and role of the autoantibodies such as IgA antiendomysium (EMA), IgA antigliadin (AGA) and the IgA antitissue transglutaminase (tTGA) in histogenesis of celiac disease. METHODS: Seventy-nine cases including 30 untreated celiacs, 5 celiacs on gluten-free diet (GFD), 41 first degree relatives and 3 non-relatives suspected for celiac disease were investigated. Three untreated celiacs with IgA deficiency were excluded from this study group. IgA antibodies to tTGA were determined by ELISA, as described before. Twelve of 41 relatives and 2 cases of non relatives suspected with positive serology underwent a small intestinal biopsy. Results were correlated with the degrees of abnormality of the intestinal mucosa in patients with celiac disease. Intestinal biopsies obtained from study population were evaluated for histological quantification. RESULTS: Celiacs and suspected cases with positive EMA/AGA and or tTGA showed shorter villi (p < 0.007) and/or a higher number of intraepithelial lymphocytes (IEL) (p < 0.035). The sensitivity of serology (EMA, AGA, tTGA) in patients with Marsh IIIc was 100%. However, in patients with Marsh IIIa the sensitivity for EMA, AGA, and tTGA was 40%, 50% and 20% respectively. CONCLUSIONS: The appearance of antibodies is related to the degree of mucosal infiltration by IELs. Although tTGA, like EMA provide a highly sensitive parameter for the detection of celiacs with severe mucosal damage, it appears to be less sensitive (even less than AGA) in celiac patients with milder histopathological abnormalities. However, it should be recognized that the substantial part of the celiac population present with these milder forms of mucosal abnormalities. Using tTGA as a single test in screening may result in missing up to 60-70% of celiacs with mild mucosal abnormalities. Combination with other screening tests (at least with AGA) is essential and strongly recommended

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